دورية أكاديمية

Knockdown of long non-coding MIR210HG inhibits cell proliferation, migration, and invasion in hepatoblastoma via the microRNA-608–FOXO6 axis

التفاصيل البيبلوغرافية
العنوان: Knockdown of long non-coding MIR210HG inhibits cell proliferation, migration, and invasion in hepatoblastoma via the microRNA-608–FOXO6 axis
المؤلفون: Yuhe Duan, He Wu, Xiwei Hao, Fujiang Li, Jie Liu, Chengzhan Zhu, Qian Dong
المصدر: Journal of International Medical Research, Vol 49 (2021)
بيانات النشر: SAGE Publishing, 2021.
سنة النشر: 2021
المجموعة: LCC:Medicine (General)
مصطلحات موضوعية: Medicine (General), R5-920
الوصف: Objective Hepatoblastoma is the most common liver tumor. Recent research has found that long non-coding (lnc)RNAs are involved in multiple types of cancers, but the potential mechanism of lncRNA MIR210HG in hepatoblastoma remains unknown. The present study explored the molecular mechanism of MIR210HG in hepatoblastoma progression. Methods The cell counting kit-8 was used to detect cell viability, and Transwell assays assessed cell migration and invasion. Luciferase reporter assays showed the relationship between MIR210HG and microRNA (miR)-608 and between miR-608 and forkhead box O6 (FOXO6). Functional tests were verified in vivo by a tumor xenograft model. The expression of MIR210HG, miR-608, FOXO6, E-cadherin, N-cadherin, and vimentin was determined by quantitative reverse transcription polymerase chain reaction and western blotting. Results MIR210HG was shown to be highly expressed in hepatoblastoma tissues and cell lines. Knockdown of MIR210HG reduced proliferation, migration, and invasion in liver cancer cells, and suppressed tumor growth in vivo . MIR210HG competitively combined with miR-608, and miR-608 decreased FOXO6 expression. Conclusion Our study demonstrated that knockdown of MIR210HG inhibits hepatoblastoma development through binding to miR-608 and downregulating FOXO6. Our results provide novel insights for hepatoblastoma treatment involving the MIR210HG–miR608–FOXO6 axis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1473-2300
03000605
Relation: https://doaj.org/toc/1473-2300
DOI: 10.1177/03000605211054695
URL الوصول: https://doaj.org/article/099a9854ebeb4757873370f7292247d3
رقم الأكسشن: edsdoj.099a9854ebeb4757873370f7292247d3
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14732300
03000605
DOI:10.1177/03000605211054695